大鼠肾血管性高血压心肌肥厚的产生和逆转  

DEVELOPMENT AND REVERSAL OF CARDIAC HYPERTROPHY IN RENOVASCULAR HYPERTENSIVE RATS

作　　者：丁小凌[1] 李云霞[1] 

机构地区：[1]湖南医科大学心血管生理研究室

出　　处：《湖南医科大学学报》1989年第3期209-212,共4页Bulletin of Hunan Medical University

基　　金：国家自然科学基金

摘　　要：用改良脑银夹使左肾动脉缩窄及切除缺血肾的方法建立大鼠肾血管性高血压产生及逆转模型,观察结果表明,孔径0.30mm银夹缩窄左肾动脉造成动脉血压持续显著升高,高血压发生率82％。第8周左心室明显肥厚,肥厚程度与高血压水平正相关。切去左肾能迅速有效地控制高血压状态,8周后心肌肥厚显著消退,但尚未完全逆转到对照水平。Renovascular hypertension was induced by left renal artery constricition and normotension was made by removal of the ischemic kidney. Their effects on the development and reversal of cardiac hypertrophy were investigated. The results showed that persistent hypertension was produced by placing a silver clip with a 0.30 mm internal diameter around left renal artery in rats.There was a significant left ventricular hypertrophy in the rats for 8 wk hypertension, in which a positive correlation between ventricular weight to body weight ratio and systolic blood pressure was observed. Removal of the ischemic kidney resulted in normotension within 24 hours, and great reversal of the hypertrophy in 8 wk later.

关 键 词：高血压 疾病模型 心脏扩大 大鼠 

分 类 号：R540.2[医药卫生—心血管疾病]